Nuclear penetration of the cyclic AMP receptor complex, new phosphorylation of a non-histone nuclear protein, and growth arrest are the sequential events that occur in hormone-dependent mammary tumors following hormone removal (ovariectomy) or dibutyryl cyclic AMP treatment of the host. Arginine, which appears to protect the cyclic AMP receptor from proteolytic attack, shows a synergistic effect with cyclic AMP both in vivo and in vitro. It is proposed that nuclear translocation of a ternary complex, cyclic AMP - phosphoreceptor - protein kinase catalytic subunit, triggers hormone-dependent mammary tumor regression.